Evidence map›Paper›PMID 23754802›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

Lhcgr expression in granulosa cells: roles for PKA-phosphorylated β-catenin, TCF3, and FOXO1.

Nathan C Law, Jennifer Weck, Brandon Kyriss, John H Nilson, Mary Hunzicker-Dunn

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. AKAP13 Enhances CREB1 Activation by FSH in Granulosa Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Periovulatory insulin signaling is essential for ovulation, granulosa cell differentiation, and female fertility.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Nathan C LawSchool of Molecular Biosciences, Washington State University, Pullman, Washington 99164-7520, USA.
Jennifer Weck
Brandon Kyriss
John H Nilson
Mary Hunzicker-Dunn
Washington State University · US

Funding

FSH-Stimulated Signals that Regulate Follicular MaturationR01HD062053 · NICHD · WASHINGTON STATE UNIVERSITY · PI HUNZICKER-DUNN, MARY E, NILSON, JOHN H. · 2009 to 2013
$1.5M
NICHD NIH HHS R01 HD062053NICHD NIH HHS R01HD62503
6 · The paper itself

Abstract

Ovarian follicles lacking FSH or FSH receptors fail to progress to a preovulatory stage, resulting in infertility. One hallmark of the preovulatory follicle is the presence of luteinizing hormone/choriogonadotropin receptors (LHCGR) on granulosa cells (GCs). However, the mechanisms by which FSH induces Lhcgr gene expression are poorly understood. Our results show that protein kinase A (PKA) and phosphoinositide 3-kinase (PI3K)/AKT pathways are required for FSH to activate both the murine Lhcgr-luciferase reporter and expression of Lhcgr mRNA in rat GCs. Based on results showing that an adenovirus (Ad) expressing a steroidogenic factor 1 (SF1) mutant that cannot bind β-catenin abolished FSH-induced Lhcgr mRNA, we evaluated the role of β-catenin in the regulation of Lhcgr gene expression. FSH promoted the PKA-dependent, PI3K-independent phosphorylation of β-catenin on Ser552 and Ser665. FSH activated the β-catenin/T-cell factor (TCF) artificial promoter-reporter TOPFlash via a PKA-dependent, PI3K-independent pathway, and dominant-negative (DN) TCF abolished FSH-activated Lhcgr-luciferase reporter and induction of Lhcgr mRNA. Microarray analysis of GCs treated with Ad-DN-TCF and FSH identified the Lhcgr as the most down-regulated gene. Chromatin immunoprecipitation results placed β-catenin phosphorylated on Ser552 and Ser675 and SF1 on the Lhcgr promoter in FSH-treated GCs; TCF3 was constitutively associated with the Lhcgr promoter. Transduction with an Ad-phospho-β-catenin mutant (Ser552/665/Asp) enhanced Lhcgr mRNA expression in FSH-treated cells greater than 3-fold. Finally, we identified a recognized PI3K/AKT target, forkhead box O1, as a negative regulator of Lhcgr mRNA expression. These results provide new understanding of the complex regulation of Lhcgr gene expression in GCs.

Indexed as

Animalsbeta CateninCells, CulturedCyclic AMP-Dependent Protein KinasesDown-RegulationFemaleFollicle Stimulating HormoneForkhead Box Protein O1Forkhead Transcription FactorsGene Expression RegulationGranulosa CellsNerve Tissue ProteinsOvarian FolliclePhosphatidylinositol 3-KinasesPhosphorylationPromoter Regions, Geneticbeta CateninCyclic AMP-Dependent Protein KinasesFollicle Stimulating HormoneForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, ratNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, GonadotropinReceptors, LHRNA, MessengerSteroidogenic Factor 1Transcription Factor 7-Like 1 Protein

Identifiers

PMID23754802
PMCPMC3725343
OpenAlexW2054506041

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.